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Role of Oxygen Metabolite in the Oxygen Paradox in Hypoxic Myocardium
저산소 심장의 oxygen paradox시 산소대사물의 역할

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Authors
Lee, Sang Dong; Choi, Chul Hee; Park, Jong Wan; Kim, Yong Sik
Issue Date
1987-09
Publisher
Seoul National University College of Medicine
Citation
Seoul J Med, Vol.28 No.3, pp. 181-188
Keywords
Hypoxic myocardiumOxygen paradoxOxygen free radicalLipid peroxidafion
Abstract
The study was conducted to confirm the hypothesis that cytotoxic oxygen free
radicals are involved in myocardial cellular damage upon reoxygenation of hypoxic hearts(oxygen
paradox), and to identify which species of oxygen radicals might be responsible for the
damage.
Oxygen paradox was induced in isolated, Langendorff preparations of rat heart by hypoxic,
cardioplegic perfusion(90 min) followed by oxygen-repleted perfusion(20 min). The releases
of cytosolic enzymes(creatine phosphokinase, CPK: lactic dehydrogenase, LDH) and a lipid
peroxidation product, malondialdehyde (MDA) into the coronary effluent were assayed as the
indicators of myocardial cellular damage. To confirm the generation of oxygen radicals during
the process of oxygen paradox, HzOz relaesed into the coronary effluent was detected using a
fluorescent dichlorofluorescln. assay.
The releases of CPK, LDH and MOA into the coronary effluent were abruptly increased by
reoxygenation in isolated hypoxic rat hearts. The concentration of HzOz detected in the
coronary effluent was also markedly elevated upon reoxygenation. The increases of enzymes
and a lipid peroxidation product were prevented to various degrees by scavengers of O2
(superoxide dismutase, 500, 10,000 U), HzOz (catalase, 25,000 U) and OH· (dimethylsulfoxide,
DMSO, 10%), and by an iron-chelator deferoxamine (0.5 mM). HzOz in the coronary
effluent increased dramatically with the adminstration of SOD in the perfusion solutions, while
it was never detected when catalase was given.
It was concluded from these results that the generation of oxygen free radicals increased
during the process of oxygen paradox in hypoxic hearts, and that the hydroxyl radical might
play a major contributing role in the development of the myocardial cellular damage through
the lipid peroxidation of cell membranes.
ISSN
0582-6802
Language
English
URI
https://hdl.handle.net/10371/6438
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Medicine (의학과)The Seoul Journal of MedicineThe Seoul Journal of Medicine Vol. 28 No.3 (1987)
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